[magnetaress]

Vaccines zero percent effective against:

Blood Agents
The principal blood agents are hydrogen cyanide (AC; HCN) and cyanogen chloride (CK; NCCl). These agents are Schedule 3 toxic chemicals according to the CWC. Schedule 3A substances have legitimate, large-scale industrial uses; therefore, large stockpiles are likely to be available for repurposing as CWAs.

Cyanide is one of the least toxic of the lethal CWAs. The inhalational LCt50 values for AC and CK have been estimated to be 2,500–5,000 and 11,000 mg min/m3, respectively (Simeonova, 2004). The cyanide ion (CN−) is the toxic moiety, mediated primarily by its great affinity for the heme a3 moiety of cytochrome c-oxidase in mitochondria, a key component in oxidative respiration. This interaction blocks the last stage in the electron transfer chain, resulting in cellular hypoxia and a shift of aerobic to anaerobic cellular respiration, leading to cellular ATP depletion and lactic acidosis. Therefore, tissues with high metabolic demands, such as neurons and cardiac cells, are key targets for toxicity. At lethal doses, death occurs within 6–8 min (Sidell et al., 1997).

Exposure to the blood agents can have two distinct effects on the eye, depending on the route of exposure. The retina and optic nerve are principal symptomatic targets of acute systemic cyanide exposure, with mydriasis commonly occurring at sublethal cyanide exposure and vision failure developing at higher doses. This is due to the metabolic inhibition of highly active neurons secondary to vascular distribution of the CN− ion. The appearance of fixed and dilated pupils is common late in the toxidromic progression, but this is likely to result from the general loss of autonomic neuronal function rather than ocular-specific toxicity (Grant and Schuman, 1993).

Alternatively, topical administration of blood agents to the ocular surface results in local absorption and toxicity, primarily concentrated in anterior ocular tissues such as the conjunctiva and lacrimal glands. Thus, topical exposure to the blood agents elicits mild ocular symptoms, primarily characterized by lacrimation and conjunctival irritation. In animal studies, the administration of sodium cyanide (1.7–5.3 mg/kg/day) to the inferior conjunctival sacs of rabbits resulted in immediate conjunctival irritation and lacrimation (Ballantyne, 1983b). In a separate study, rabbits that were administered 0.9 mg/kg of hydrogen cyanide to the conjunctival sacs were reported to develop general keratitis (Ballantyne, 1983a). These two experiments involved the administration of lethal doses of cyanide in liquid form directly to the conjunctiva, which is likely to lead to the very rapid cytotoxicity of local nerves, blood vessels, and epithelial cells. Exposure to sublethal concentrations of cyanogen chloride vapor similarly caused intense conjunctival irritation, severe blepharospasm, and lacrimation.

Exposure Physiology
The cyanides, formerly known as “blood agents,” consist of hydrogen cyanide (NATO code designation AC, HCN: MW 27.04) and cyanogen chloride (CK, ClCN: MW 61.5). The common metabolic by-product is the toxic CN− anion, which is largely a systemic toxicant. Vapors from these agents are heavier than air and spread across the ground like phosgene and can pose a problem in low-lying, confined areas (Table 36.1). A mild exposure to these agents through the inhalation route can cause headache, loss of consciousness, ataxia, and confusion. Palpitations and respiratory tract irritation with labored breathing (dyspnea) can lead to hyperpnea in some cases. For exposures classified as severe, serious CNS effects may occur. These include coma, seizures, and mydriasis. Dysrhythmias, low blood pressure, and eventual life-threatening cardiac arrest may follow. The occurrence of pulmonary edema followed by respiratory insufficiency can be a late manifestation following a severe inhalation exposure episode. The toxic load of inhaled HCN can be enhanced through its effect on increased minute volume (Purser et al., 1984).

Animal studies have provided evidence of the tissue distribution of inhaled cyanide. These studies have indicated that the target organs are the lung and heart, followed by the brain; all highly perfused. For example, in the rat following an acute inhalation exposure to HCN, the highest concentrations were measured in the blood, brain, heart, and lung with very little in the liver (Ballantyne, 1994). The estimated human inhaled 50% lethal concentration of HCN is 2,500–5,000 mg×min/m3 and for cyanogen chloride, it is approximately 11,000 mg×min/m3. These data indicate that via the inhalation route, the cyanides are less toxic compared to their effects as systemic poisons (McNamara, 1976).

Betting CoVID 19 is a biological warfare form of said poison. And a lot of testing was done on 'dissemination' or effective spread among populations. Blood agents that linger, absolutely fucking hilariously lulz - no more anthropogenic global warming for at least 10 thousand years. The highly lethal strain being held back in leiu of scaring the piss out of the enemy elites and holding them hostage whilst collecting data and avoiding full scale economic collapse, which would have required their own slaves to be put down as they would have become excess without an overseas market.

1976 was when the results of many secret studies started becoming public, think about it for a minute and then go have a cigarrete.

Overall a pretty good beta test and threat to make the UN/NATO powers play ball during a point where they were weakened by political infighting in the US. -- so a low threat of retaliation.